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Year : 2021  |  Volume : 69  |  Issue : 4  |  Page : 1048--1050

Unilateral Basal Ganglia Hyperintensity Secondary to Venous Congestion in a Case of Indirect Carotico-cavernous Fistula

Suresh Giragani1, Ashok Reddy Kasireddy1, Vikas Agrawal2, Swathi Muthyala1,  
1 Department of Neuroradiology and Interventional Radiology, Yashoda Hospitals, Alexander Road, Secunderabad, Telangana, India
2 Department of Neurology, Yashoda Hospitals, Alexander Road, Secunderabad, Telangana, India

Correspondence Address:
Suresh Giragani
Department of Neuroradiology and Interventional Radiology, Yashoda Hospitals, Alexander Road, Secunderabad, Telangana 500003


Intraparenchymal venous congestive changes secondary to carotico-cavernous fistula are not common. Isolated basal ganglia venous congestive changes in carotico-cavernous fistula have been rarely described. We report MRI findings of the unilateral basal ganglia hyperintensity, angiographic features including cortical venous reflux into a variant basal vein of Rosenthal, in a postpartum woman presenting with the left eye proptosis and the right upper limb weakness. We also describe the reversal of imaging findings and resolution of patients' symptoms after definitive treatment of the carotico-cavernous fistula by endovascular embolization

How to cite this article:
Giragani S, Kasireddy AR, Agrawal V, Muthyala S. Unilateral Basal Ganglia Hyperintensity Secondary to Venous Congestion in a Case of Indirect Carotico-cavernous Fistula.Neurol India 2021;69:1048-1050

How to cite this URL:
Giragani S, Kasireddy AR, Agrawal V, Muthyala S. Unilateral Basal Ganglia Hyperintensity Secondary to Venous Congestion in a Case of Indirect Carotico-cavernous Fistula. Neurol India [serial online] 2021 [cited 2021 Oct 22 ];69:1048-1050
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Full Text

An indirect carotid cavernous fistula (CCF) is a type of dural arterio venous fistula that results from an abnormal communication between the meningeal branches of internal carotid artery, external carotid arteries, and cavernous sinus in the skull base.[1] Clinical manifestations of CCF depend upon preferential venous drainage pathway effected secondary to the venous hypertension.[2] Usually, patients with CCF present with proptosis, chemosis, cranial nerve palsies etc. Very rarely they can present with venous congestive changes in brainstem and basal ganglia secondary to venous reflux in the lateral mesencephalic vein or an anomalous basal vein of Rosenthal (BVR).[3],[4] In this report, we wish to describe the isolated venous congestive changes in basal ganglia secondary to indirect carotico-cavernous fistula.

 Case Presentation

A 28-year-old woman who had recent normal vaginal delivery presented with complaints of proptosis of the left eye, double vision, and weakness in the right upper limb for 3 days. On examination, there was left eye proptosis, chemosis with oculomotor nerve palsy; and she was not able to lift her right hand against gravity. A contrast-enhanced magnetic resonance imaging of brain and orbits was performed, which revealed T2 hyperintense signal involving the left lentiform nucleus, internal capsule, and caudate nucleus. The diffusion-weighted images show bright signal in the left caudate nucleus. The left cavernous sinus was showing flow related enhancement with post contrast diffuse nodular enhancement. The left superior ophthalmic vein was dilated [Figure 1]. There was associated diffuse enhancement of the extraocular muscles of the left eye with myofascial and retro orbital fat stranding. Further, a digital subtraction angiography was performed, which revealed presence of a Barrow's Type D indirect CCF involving left cavernous sinus with arterial feeders from deep temporal artery, artery of foramen rotundum, and pterygoid branches of left internal maxillary artery and meningo hypophyseal branches of left cavernous ICA. The venous drainage was preferentially superiorly and anteriorly. Posteriorly, the inferior and superior petrosal sinuses were not patent. Superiorly venous reflux was noted into the first segment of BVR and further into the left-sided striate veins [Figure 2]. The second and third parts of BVR were seen in their entirety however small in caliber, which are seen to drain into the vein of Galen (VOG). After consent, endovascular embolisation of the fistula was planned under general anesthesia. Because of occluded inferior petrosal sinus, initially left angular vein approach was attempted. However, due to tortuous junction of superior ophthalmic vein and angular vein, the cavernous sinus could not be accessed. Hence, a trans arterial approach was performed. The fistula was accessed from deep temporal artery branch of the left internal maxillary artery with Marathon micro catheter (ev3, Irvine, CA, USA) and 0.008″ mirage guide wire (ev3, Irvine, CA, USA) and embolized with liquid embolizing agent Onyx-18 (ev3, Irvine, CA, USA). Complete angiographic obliteration of the fistula was achieved [Figure 3]. At 1-month clinical follow-up, the patient had normal power in her right upper limb and a complete resolution of proptosis. On follow-up MRI at three months, there was resolution of basal ganglia hyperintensity.{Figure 1}{Figure 2}{Figure 3}


Indirect CCFs are usually low flow arteriovenous shunts between the meningeal branches of either the ICA or ECA and cavernous sinus.[1] The clinical manifestations and the aggressiveness of CCF are dependent predominantly on the routes of venous drainage. Clinically, patients with CCF usually present with proptosis and chemosis secondary to engorgement of the superior ophthalmic vein draining the arterialized cavernous sinus.[2] Intraparenchymal hemorrhage and venous infarction have been described in CCF associated with cortical venous reflux.[5] The venous congestion changes had been predominantly described in the brainstem and basal ganglia in the setting of venous reflux into anatomical variant of BVR. Although more extensive combined basal ganglia and brainstem congestive changes have been described in CCF,[4] selective isolated venous congestion edema in basal ganglia secondary to the CCF has not been described in the literature.

The BVR are two in number, formed by the union of inferior striate vein, anterior cerebral vein, and deep middle cerebral vein. It originates at the medial edge of temporal lobe and passes in ambient cistern to join the Great (VOG). Huang and Wolf classified BVR into three anatomical segments.[6] The first segment extends from the union of the inferior striate vein, the anterior cerebral vein, and the deep middle cerebral vein to the anterior end of cerebral peduncle. The insular veins drain into deep middle cerebral vein. The second segment extends from the cerebral peduncle to the union of the BVR with the lateral mesencephalic vein, and the third segment extends from the end of second segment to the great VOG. If any of the three segments may be hypoplastic and drainage will be redirected into cavernous sinus, superior petrosal sinus, or transverse sinus accordingly.[6] Suzuki et al. studied anatomical variations of BVR in about 250 patients (500 sides).[7] The anastomosis between the first segment and second segment were not visualized in 36.9% of cases. The first segments with such hypoplastic or aplastic anastomosis flowed into the cavernous sinus or spheno parietal sinus, whereas the second and third segments drained into VOG.[7] Also, more than one-fourth of cases with the typical type, i.e. with anastomosis between all three segments which are entering into VOG, also entered anterior sinuses or veins such as the cavernous sinus. Our index case demonstrated BVR with all three segments anastomosing with each other with drainage into VOG. However, the first segment of BVR is seen to anastomose also with the left cavernous sinus, which was dilated due to reflux from the cavernous sinus secondary to fistula. Since first segment of the BVR drains the inferior striate veins, anterior cerebral veins, and uncal veins, engorgement of this segment by the CCF explains the signal abnormalities in basal ganglia in the MRI.

The direction of venous egress may not be static; it can evolve over time with the development of venous occlusions and venous rerouting as a result of progressive venous restrictive angiopathic changes and gradual thrombosis.[8] In the index case, the prothrombotic state induced by postpartum status may have caused an acute occlusion of petrosal sinuses.[9] Probably this restricted outflow must have led to selective venous reflux anteriorly into SOV and superiorly into the inferior striate vein tributary of the BVR via the prominent uncal vein resulting in venous congestion in the basal ganglia. Intact although smaller second and third parts BVR may have led to sparing of posterior structures including brainstem from venous congestion, the reversibility of basal ganglia changes after the embolization of CCF further confirm the etiopathogenesis.


Venous congestion manifesting as isolated basal ganglia hyperintensity is a rare imaging finding in CCF. The association of cavernous sinus arterialization, a prominent uncal vein with reflux into striate tributaries of BVR, a thrombosed or hypoplastic inferior, and superior petrosal sinuses may explain this rare manifestation of indirect CCF. Knowledge and awareness of this unusual imaging finding in CCF may help in early diagnosis and treatment of this condition.

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Conflicts of interest

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